1NMR Laboratory, Institute of Myology,
F-75651 Paris, France; 2CEA, IBM, MIRCen, IdM NMR Laboratory,
F-75651 Paris, France; 3Unite de Diabetologie et Nutrition,
Universite Catholique de louvain, B-1200 Brussels, Belgium
Inhibiting
myostatin (mstn) causes spectacular increase in muscle mass, and has opened
the path to therapeutic approaches. Yet possible compromised force production
have been reported in isolated muscle. We investigated vascular and metabolic
response to exercise in vivo in mstn-/- and wild-type mice using interleaved
arterial spin labeling NMR imaging and 31P spectroscopy. Specific force and
maximum perfusion were identical. Mitochondrial oxidative capacities were
reduced in mstn-/-, while hyperemia was prolonged. These integrated results
formed coherent evidence of a non-pathologic shift towards a more glycolytic
metabolism in this model as was confirmed by histology.